RRC ID 51458
著者 Rojo Romanos T, Pladevall-Morera D, Langebeck-Jensen K, Hansen S, Ng L, Pocock R.
タイトル LIN-32/Atonal Controls Oxygen Sensing Neuron Development in Caenorhabditis elegans.
ジャーナル Sci Rep
Abstract Development of complex nervous systems requires precisely controlled neurogenesis. The generation and specification of neurons occur through the transcriptional and post-transcriptional control of complex regulatory networks. In vertebrates and invertebrates, the proneural basic-helix-loop-helix (bHLH) family of transcription factors has multiple functions in neurogenesis. Here, we identified the LIN-32/Atonal bHLH transcription factor as a key regulator of URXL/R oxygen-sensing neuron development in Caenorhabditis elegans. When LIN-32/Atonal expression is lost, the expression of URX specification and terminal differentiation genes is abrogated. As such, lin-32 mutant animals are unable to respond to increases in environmental oxygen. The URX neurons are generated from a branch of the cell lineage that also produces the CEPDL/R and URADL/R neurons. We found development of these neurons is also defective, suggesting that LIN-32/Atonal regulates neuronal development of the entire lineage. Finally, our results show that aspects of URX neuronal fate are partially restored in lin-32 mutant animals when the apoptosis pathway is inhibited. This suggests that, as in other organisms, LIN-32/Atonal regulates neuronal apoptosis.
巻・号 7(1)
ページ 7294
公開日 2017-8-4
DOI 10.1038/s41598-017-07876-4
PII 10.1038/s41598-017-07876-4
PMID 28779171
PMC PMC5544745
MeSH Animals Caenorhabditis elegans / physiology* Caenorhabditis elegans Proteins / genetics Caenorhabditis elegans Proteins / metabolism* Gene Expression Genes, Reporter Mutation Neurogenesis* Neurons / metabolism* Oxygen / metabolism* Transcription Factors / genetics Transcription Factors / metabolism*
IF 3.998
引用数 1
リソース情報
線虫 tm1446 tm1768